Metabolic and mitochondrial treatments for severe paracetamol poisoning: a systematic review

Mullins, M. E. and Yeager, L. H. and Freeman, W. E.

Clinical Toxicology (2020) 58: 1284–1296

DOI: 10.1080/15563650.2020.1798979

Abstract

Background: Paracetamol (acetaminophen) remains a leading cause of poisoning in Europe, North America, and Australia. For over four decades, acetylcysteine has been the antidote of choice. However, despite the use of acetylcysteine, some patients who ingest very large doses of paracetamol or who reach hospital late in the course of their poisoning, develop acute liver failure. Some will develop metabolic acidosis indicating mitochondrial toxicity.

Citation

Mullins, M. E., Yeager, L. H., & Freeman, W. E. (2020). Metabolic and mitochondrial treatments for severe paracetamol poisoning: a systematic review. Clinical Toxicology, 58(12), 1284–1296. https://doi.org/10.1080/15563650.2020.1798979 acetaminophen, animal models, man, systematic reviews, human diseases, drug therapy, antidotes, chemotherapy, Animal and in vitro Models for Pharmaceuticals [VV450], Animal Models of Human Diseases [VV400], Pharmacology [VV730], drug toxicity, superoxide dismutase, Human Toxicology and Poisoning [VV810], mitochondria, poisoning, toxicosis, mode of action, free radicals, acetylcysteine, calmangafodipir, cimetidine, cytochrome P-450, fomepizole, overdose, paracetamol

Keywords

• acetaminophen
• animal models
• man
• systematic reviews
• human diseases
• drug therapy
• antidotes
• chemotherapy
• Animal and in vitro Models for Pharmaceuticals [VV450]
• Animal Models of Human Diseases [VV400]
• Pharmacology [VV730]
• drug toxicity
• superoxide dismutase
• Human Toxicology and Poisoning [VV810]
• mitochondria
• poisoning
• toxicosis
• mode of action
• free radicals
• acetylcysteine
• calmangafodipir
• cimetidine
• cytochrome P-450
• fomepizole
• overdose
• paracetamol